Chantal Bolduc

Hair care products: waving, straightening, conditioning, and coloring

Hair is a very important and distinctive feature that plays a major role in self perception. To some extent, it expresses our personality and who we are. Hair is one of the few physical features that we can easily change. Its length, color, and shape can be modified to create a totally different style. All those different styles can be used to seduce, conform, or even make a statement. Although hair has no vital function, its immeasurable importance is usually brutally discovered by those affected by alopecia. Although hair cosmetics are widely available, the medical literature is rather scarce, and specialized literature is not readily accessible to most of us. The aim of this article is to give a practical and simple overview of the different hair cosmetic treatments available. Knowing how they affect the hair will enable the physician to better assess different problems secondary to cosmetic treatments and will also provide some answers to commonly asked questions.

Localized hyperhidrosis treated with aluminum chloride in a salicylic acid gel base

A total of 238 patients with a clinical diagnosis of localized hyperhidrosis (HH) were treated on 332 anatomic sites (axillae, feet, hands, and groin). The purpose of the study was to evaluate the effectiveness of aluminum chloride hexahydrate (AC), in a salicylic acid gel base (SAGB) containing 4% salicylic acid (SA), for the treatment of localized HH. The SAGB was similar to a keratolytic gel, 1 Keralyt® (Westwood Squibb). Because SAGB and anhydrous alcohol (AA), the standard vehicle for AC, have different consistencies, double blinding was not possible. Bromhidrosis (BH) was documented when present, whether of apocrine (axillae and groin) or eccrine (feet) origin. For the sake of uniformity, AC in SAGB was compounded by the same pharmacist. The concentration of AC varied from 10 to 40%, depending on the site to be treated. The improvement of HH was subjectively assessed through a questionnaire as follows: nil = no improvement; poor = <25%; fair = 25–50%; good = 50–75%; and excellent = >75%.

Effects of the tumor necrosis factor-α antagonist adalimumab on arterial inflammation assessed by positron emission tomography in patients with psoriasis: results of a randomized controlled trial.

Background—Psoriasis is a chronic inflammatory disease associated with increased risks of myocardial infarction and stroke. Systemic treatments for moderate to severe psoriasis can reduce skin and joint inflammation; however, their effects on vascular inflammation are unknown. Methods and Results—This randomized, controlled trial included 30 patients with moderate to severe psoriasis and a history, or multiple risk factors, of coronary atherosclerosis. Patients were randomized (2:1) to receive either adalimumab subcutaneously for 4 months or to control nonsystemic treatment (topical therapies or phototherapy). Vascular inflammation was measured in the carotid artery and ascending aorta at baseline and week 15, by 18F-fluorodeoxyglucose uptake on positron emission tomography. The change in target:background ratio in the vessel with highest baseline target:background ratio (primary end point) was significant at week 15 compared with baseline for patients randomized to adalimumab (–0.23 [95% CI, –0.39 to –0.08]; P=0.004) but not for the control group (–0.10 [95% CI, –0.32 to 0.12]; P=0.35). The difference between study arms for this primary end point did not reach statistical significance (–0.13 [95% CI, –0.01 to 0.14]; P=0.32). The change in target:background ratio at week 15 improved with adalimumab compared with controls both in the ascending aorta (–0.26±0.11, P=0.021) and in carotid arteries (–0.32±0.15, P=0.037) when analyzed separately (secondary end points). Changes in other positron emission tomography indices also improved significantly with adalimumab compared with controls in the ascending aorta and carotids. High-sensitivity C-reactive protein decreased by 51% at week 16 with adalimumab compared with 5% in controls (P=0·002). Conclusions—The study did not meet its primary end point because the change in target:background ratio in patients randomized to adalimumab was not different from controls. Although adalimumab may reduce vascular inflammation in patients with moderate to severe psoriasis, this effect is not large enough to be demonstrated in a study with a small sample size. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NTC00940862.

Efficacy and safety of adalimumab in patients with plaque psoriasis who have shown an unsatisfactory response to etanercept

BACKGROUND The safety and efficacy of adalimumab in patients who have shown an unsatisfactory response to etanercept are unknown. OBJECTIVE We sought to evaluate the safety and efficacy of adalimumab in patients who failed to show a satisfactory response or lost their satisfactory response to etanercept. METHODS This multicenter study enrolled patients who either failed to reach a physician global assessment (PGA) score of 0 or 1 after 12 weeks of etanercept (group A; 50 patients) or who lost their PGA score of 0 or 1 at any time after etanercept dose decrease from 50 mg twice a week to 50 mg every week (group B; 35 patients). Patients received adalimumab 40 mg every other week without loading dose for 12 weeks followed by 40 mg every week for an additional 12 weeks if they did not reach a PGA score of 0 or 1. RESULTS After 12 weeks of adalimumab, 34.0% (n = 17; 95% confidence interval [CI] 20.4-47.6) and 31.4% (n = 11; 95% CI 15.2-47.6) of patients from groups A and B, respectively, reached a PGA score of 0 or 1. A total of 46.0% (n = 23; 95% CI 31.7-60.3) and 45.7% (n = 16; 95% CI 28.4-63.1) of patients from group A and B, respectively, achieved a PGA score of 0 or 1 after 24 weeks of adalimumab. Adalimumab was well tolerated and no serious adverse events were reported. LIMITATIONS This was an open-label uncontrolled study. CONCLUSIONS Adalimumab should be considered as an alternative in patients with psoriasis who have not shown an adequate response or who lost their response to etanercept after a dose decrease.

Effects of the TNF alpha Antagonist Adalimumab on Arterial Inflammation Assessed by Positron Emission Tomography in Patients with Psoriasis: Results of a Randomized Controlled Trial

Background—Psoriasis is a chronic inflammatory disease associated with increased risks of myocardial infarction and stroke. Systemic treatments for moderate to severe psoriasis can reduce skin and joint inflammation; however, their effects on vascular inflammation are unknown. Methods and Results—This randomized, controlled trial included 30 patients with moderate to severe psoriasis and a history, or multiple risk factors, of coronary atherosclerosis. Patients were randomized (2:1) to receive either adalimumab subcutaneously for 4 months or to control nonsystemic treatment (topical therapies or phototherapy). Vascular inflammation was measured in the carotid artery and ascending aorta at baseline and week 15, by 18F-fluorodeoxyglucose uptake on positron emission tomography. The change in target:background ratio in the vessel with highest baseline target:background ratio (primary end point) was significant at week 15 compared with baseline for patients randomized to adalimumab (–0.23 [95% CI, –0.39 to –0.08]; P=0.004) but not for the control group (–0.10 [95% CI, –0.32 to 0.12]; P=0.35). The difference between study arms for this primary end point did not reach statistical significance (–0.13 [95% CI, –0.01 to 0.14]; P=0.32). The change in target:background ratio at week 15 improved with adalimumab compared with controls both in the ascending aorta (–0.26±0.11, P=0.021) and in carotid arteries (–0.32±0.15, P=0.037) when analyzed separately (secondary end points). Changes in other positron emission tomography indices also improved significantly with adalimumab compared with controls in the ascending aorta and carotids. High-sensitivity C-reactive protein decreased by 51% at week 16 with adalimumab compared with 5% in controls (P=0·002). Conclusions—The study did not meet its primary end point because the change in target:background ratio in patients randomized to adalimumab was not different from controls. Although adalimumab may reduce vascular inflammation in patients with moderate to severe psoriasis, this effect is not large enough to be demonstrated in a study with a small sample size. Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NTC00940862.

Primary cicatricial alopecia

Both primary and secondary forms of cicatricial alopecia have been described. The hair follicles are the specific target of inflammation in primary cicatricial alopecias. Hair follicles are destroyed randomly with surrounding structures in secondary cicatricial alopecia. This 2-part continuing medical education article will review primary cicatricial alopecias according to the working classification suggested by the North American Hair Research Society. In this classification, the different entities are classified into 3 different groups according to their prominent inflammatory infiltrate (ie, lymphocytic, neutrophilic, and mixed). Part I discusses the following lymphocytic primary cicatricial alopecias: chronic cutaneous lupus erythematosus, lichen planopilaris, frontal fibrosing alopecia, and Graham-Little syndrome.

Efficacy and Safety of Adalimumab Treatment in Patients with Moderate to Severe Psoriasis: A Double-Blind, Randomized Clinical Trial

Background Tumor necrosis factor-alpha (TNF-α) is pivotal in the pathogenesis of psoriasis, an immune-mediated disease. Adalimumab is a fully human, IgG1 monoclonal antibody that inhibits TNF-α. Objectives The aims of this study were to assess the efficacy and safety of adalimumab therapy for patients with moderate to severe plaque psoriasis and evaluate the duration of treatment response after withdrawal from or dosage reduction of adalimumab therapy. Methods In this multicenter, randomized, double-blind, placebo-controlled study, patients with moderate to severe plaque psoriasis received 12-week, open-label therapy with subcutaneous adalimumab, consisting of 80 mg of adalimumab at weeks 0 and 1, followed by 40 mg weekly at weeks 2–11. At week 12, patients who had an improvement in Psoriasis Area and Severity Index (PASI) score of ≥50% were randomized to blinded therapy and received either adalimumab 40 mg every other week (eow) or placebo for an additional 12 weeks. Results A total of 148 patients enrolled. Clinical response was rapid, with a PASI 50 response rate of 28% at week 2 of adalimumab therapy. At week 12, 91.9% (136/148) of patients had achieved ≥50% reduction in PASI (PASI 50) vs. baseline, 76.4% (113/148) had achieved PASI 75, and 47.3% (70/148) had achieved PASI 90. Of patients who were randomized to placebo at week 12, 30.9% (21/68) experienced a relapse (<PASI 50 improvement vs. baseline) by week 24, compared with 16.2% (11/68) of patients who received adalimumab 40 mg eow. In addition, 48.5% (33/68) of patients who were randomized to placebo at week 12 were PASI 75 responded at week 24, compared with 67.6% (46/68) of patients randomized to adalimumab 40 mg eow (p=0.032). And, 27.9% (19/68) of patients who were randomized to placebo at week 12 were PASI 90 responders at week 24, compared with 47.1% (32/68) of patients randomized to adalimumab 40 mg eow (p=0.028). Adalimumab was generally well-tolerated, and the rates of adverse events were comparable between the adalimumab and placebo groups. Conclusions Weekly adalimumab therapy rapidly improved psoriasis during an initial 12-week period. Improvement was sustained in most, but not all patients, despite dosage reduction to every other week. No patients randomized to adalimumab withdrawal (placebo at week 12) experienced rebound, and most maintained >PASI 50 improvement, relative to baseline, during the 3 months following adalimumab discontinuation. Overall, greater efficacy rates at week 24 were observed for patients randomized to continuous adalimumab therapy than for patients who were withdrawn from therapy at week 12.

Management of Androgenetic Alopecia

Androgenetic alopecia is by far the most common cause of hair loss. It affects approximately 50% of men by the age of 50 and 20 to 53% of women by the age 50. Although it is a medically benign condition, it is a significant psychosocial issue for many patients. Various different treatment options are now available for androgenetic alopecia.The best treatment option for women with androgenetic alopecia Ludwig stage I and II is minoxidil 5% solution. If it is not effective after 1 year, antiandrogens can be tried, but there are no large studies showing their efficacy and they have considerable adverse effects. Also, for patients with alopecia that is unresponsive to treatment or with Ludwig stage III, hair transplantation can be offered if the occipital donor area is sufficient. For men, we always offer minoxidil or finasteride therapy and leave the choice of therapy to the patient. Some patients may prefer a systemic agent, whereas others may favor a topical agent. If the condition is not stabilized after 1 year or if the patient wants greater hair density, hair transplantation can be discussed.There have been tremendous advances in the treatment of hair loss in recent years and the future is very encouraging. As our knowledge of androgenetic alopecia pathophysiology increases, novel targeted treatments will potentially be developed.

Primary cicatricial alopecia: Lymphocytic primary cicatricial alopecias, including chronic cutaneous lupus erythematosus, lichen planopilaris, frontal fibrosing alopecia, and Graham-Little syndrome

Both primary and secondary forms of cicatricial alopecia have been described. The hair follicles are the specific target of inflammation in primary cicatricial alopecias. Hair follicles are destroyed randomly with surrounding structures in secondary cicatricial alopecia. This 2-part continuing medical education article will review primary cicatricial alopecias according to the working classification suggested by the North American Hair Research Society. In this classification, the different entities are classified into 3 different groups according to their prominent inflammatory infiltrate (ie, lymphocytic, neutrophilic, and mixed). Part I discusses the following lymphocytic primary cicatricial alopecias: chronic cutaneous lupus erythematosus, lichen planopilaris, frontal fibrosing alopecia, and Graham-Little syndrome.

Effect of adalimumab on sleep parameters in patients with psoriasis and obstructive sleep apnea: a randomized controlled trial

Introduction: Obstructive sleep apnea (OSA) is frequently seen in patients with psoriasis vulgaris. The effect of adalimumab, a TNF-α antagonist, on OSA is unknown. Methods: Patients with at least 5% of their body surface area covered with psoriasis and a sleep apnea defined as an apnea/hypopnea index (AHI) of at least 15 were recruited. They were randomized to either adalimumab 80 mg followed by adalimumab 40 mg every other week for 7 weeks or placebo. Patients were evaluated by polysomnography at baseline and day 56. The objective of this trial was to study the efficacy of adalimumab on sleep parameters in patients with psoriasis and OSA. The primary end point of this double-blind study was the change in AHI between baseline and day 56. Results: A total of 20 patients who were randomized completed the trial. There was no significant difference (p = 0.485) (95% CI = –21.07–42.73) at day 56 in the change from baseline in AHI between groups. Conclusions: Adalimumab used for 8 weeks at 40 mg every other week for the treatment of psoriasis did not improve OSA in this 20-patient study.